The human fungal pathogen is the major etiological agent of vulvovaginal candidiasis (VVC). Despite this fact, other non- (NAC) species have frequently been reported as well. Despite their presence in the vaginal environment, little is known about their capacity to elicit immune responses classically associated with -mediated immunopathology, including neutrophil recruitment and pro-inflammatory cytokine signaling. Therefore, using a combination of in vitro and in vivo approaches, we undertook a comparative analysis to determine whether a representative panel of NAC species could colonize, induce immunopathological markers, or cause damage at the vaginal mucosa. Using a murine model of VVC, was found to induce robust immunopathology (neutrophils, IL-1β) and elicit mucosal damage. However, all NAC species tested (including ,, ,, ,) induced significantly less damage and neutrophil recruitment, despite achieving similar early colonization levels as These results largely correlated with notable lack of the NAC species ( and included) to form hyphae both in vitro and in vivo. Furthermore, both and induced significantly less expression of the gene encoding for Candidalysin, a key fungal virulence determinant driving VVC immunopathology. In order to determine the relative capacity of these species to elicit inflammasome-dependent IL-1β release, both WT and NLRP3-/- THP-1 cells were challenged in vitro. While most species tested elicited only modest amounts of IL-1β, challenge with led to significantly elevated levels that were largely NLRP3-dependent. Collectively, our findings demonstrate that although NAC species are increasingly reported as causative agents of VVC, appears to be exceedingly vaginopathogenic, exhibiting robust immunopathology, hypha formation and Candidalysin expression. Thus, this study provides mechanistic insight as to why is overwhelmingly the major pathogen reported during VVC.